European Heart Journal (2003) 24, 801–810

Clinical and electrophysiological differences

between patients with arrhythmogenic right
ventricular dysplasia and right ventricular outflow
tract tachycardia
D. O'Donnell a*, D. Cox a, J. Bourke a, L. Mitchell b, S. Furniss a
a
Department of Cardiology, Freeman Hospital, Newcastle upon Tyne, UK
b
Department of Radiology, Freeman Hospital, Newcastle upon Tyne, UK
Received 17 August 2002; revised 6 September 2002; accepted 11 September 2002

KEYWORDS
Ventricular tachycardia;
Catheter ablation;
Cardiomyopathy
Aims Radiofrequency catheter ablation is considered first line treatment for sympto-
matic patients with right ventricular outflow tract tachycardia (RVOT). The role of
ablation in arrhythmogenic right ventricular dysplasia (ARVD) is more limited. As such,
differentiating between the two conditions is essential.
Methods and results This study compared non-invasive findings, magnetic resonance
images (MRI), invasive electrophysiological characteristics, results of ablation and
long-term outcome in 50 consecutive patients with RVOT (33) or ARVD (17). Structural
abnormalities were uniform in the ARVD group; in addition 18 (54%) of the RVOT
tachycardia group had MRI abnormalities. At electrophysiological study the tachy-
cardia in the ARVD group displayed features of re-entry in over 80%, but behaved with
a triggered automatic basis in 97% with RVOT. Ablation was complete or partial
success in 12 (71%) patients with ARVD and ventricular tachycardia (VT) recurred in
eight (48%). In the RVOT patients, ablation was a complete success in 97% with
recurrent VT in 6%. Long-term success in the RVOT patients was 95% in both patients
with and without MRI abnormalities.
Conclusions Electrophysiological characterization can differentiate ARVD from RVOT.
The finding of abnormalities on MRI does not have any bearing on arrhythmia
mechanism, acute or long-term success of RFA.
© 2003 The European Society of Cardiology. Published by Elsevier Science Ltd. All
rights reserved.

Introduction terized by right ventricular dysfunction due to

Right ventricular tachycardia is commonly due to
arrhythmogenic right ventricular dysplasia/
cardiomyopathy (ARVD) or idiopathic right ven-
tricular outflow tract (RVOT) tachycardia.1,2 ARVD
is an inherited progressive cardiomyopathy charac-
* Corresponding author. Department of Cardiology, Austin
and Repatriation Medical Center, Studley Road, Heidleberg,
Victoria 3084, Australia. Tel.: +61-3-9496-5000; fax:
+61-3-9459-0971
E-mail address: odonnell_research@hotmail.com (D. O'Donnell).
fibrofatty replacement of myocardium, predispos-
ing to ventricular tachycardia and death.3–7 Right
ventricular outflow tract tachycardia is a benign
condition, traditionally considered to be a primary
electrical disease in the absence of structural heart
disease.8–11 The differentiation between ARVD
and RVOT tachycardia is important clinically when
discussing prognosis and management options.
At the extremes of disease presentation differ-
entiating between the two conditions is usually
straightforward. However, detailed analyses using

0195-668X/03/$ - see front matter © 2003 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved.
doi:10.1016/S0195-668X(02)00654-1
802
magnetic resonance imaging (MRI),12–15 signal
averaged electrocardiograms1,11 and endomyo-
cardial biopsy1 have detected structural abnormali-
ties in patients with RVOT tachycardia, which are
similar to those seen in the early stages of ARVD.
These findings have made the differentiation of
ARVD and RVOT tachycardia at the time of initial
diagnosis more difficult in some patients. It is
unclear whether the two conditions represent
separate entities or together form a continuous
spectrum of disease, with ROVT tachycardia repre-
senting a concealed or early form of ARVD. The
clinical and prognostic significance of the structural
abnormalities detected with newer technologies is
uncertain.
The aim of this study was to compare the two
conditions with regard to the demographic, elec-
trocardiographic, structural and invasive electro-
physiological characteristics, in patients with ARVD
or RVOT tachycardia. These findings were also
analysed to identify any correlation with the acute
or longer term success of radiofrequency ablation.
Methods
Patients
This study analysed details of 50 consecutive
patients with right ventricular tachycardia, in the
absence of coronary disease, surgical scars or left
ventricular dysfunction, who were scheduled to
undergo electrophysiological study and radio-
frequency ablation. The right ventricular origin was
determined by electrocardiographic criteria and
confirmed in all cases at electrophysiological study.
The patients were prospectively diagnosed as ARVD
or RVOT tachycardia, according to guidelines
published by the Study Group on ARVD/C of the
Working Group of Myocardial and Pericardial
Diseases of the European Society of Cardiology
and of the Scientific Council on Cardiomyopathies
of the International Society and Federation of
Cardiology.16 This classification takes account of
genetic, electrocardiographic depolarization and
repolarization, arrhythmic, structural and histo-
logical factors. Based on this classification, the
diagnosis of ARVD requires the presence of two
major criteria or one major and two minor criteria
or four minor criteria.
Electrocardiographic analysis
A standard 12-lead electrocardiogram was recorded
during sinus rhythm free from anti-arrhythmic drug
D. O'Donnell et al.
effects. The QRS/T complex in V1–3 was examined
for the presence of epsilon waves, right bundle
branch block and T wave inversion. QRS and
QT measurements were made using a Calcomp
Digitizer from electrocardiograms recorded at a
paper speed of 50 mm s−1.
Signal averaged electrocardiograms were ob-
tained using a Marquette MAC VU system. Record-
ings were made during sinus rhythm using standard
Frank leads X, Y and Z. Two hundred and fifty beats
were averaged to obtain a noise level of <0.3 µV.
The signals were amplified, averaged and filtered
with a bidirectional filter at frequencies of 40–
250 Hz. The duration of the total filtered QRS
complex, the duration of the filtered QRS complex
after the voltage decreased to <40 mV, and the root
mean square of the amplitude of signals in the last
40 ms of the filtered QRS complex were measured
by a computer algorithm. Results were deemed
abnormal if any two of the following criteria were
met: (1) the filtered QRS duration was ≥120 ms; (2)
the duration of the filtered QRS complex after the
voltage decreased to <40 mV, was >40 ms; (3) the
root mean square of the voltage in the last 40 ms of
the QRS complex was <20 mV.
Ventricular tachycardia morphology was ob-
tained either from a 12-lead electrocardiogram
recording during sustained ventricular tachycardia
or from an electrocardiogram with consistent
monomorphic ventricular ectopic beats.
Structural analysis
Transthoracic echocardiography
All patients underwent transthoracic echocardiog-
raphy prior to the study, which was reported by a
cardiologist blinded to the clinical details. The
focus on the right ventricle included measurements
of overall right ventricular size and function, as
well as a description of localized right ventricular
aneurysms, segmental dilatation or regional wall
motion abnormalities.
Magnetic resonance imaging
MRI of the heart was performed according to a
standardized technique in all patients. Scans were
performed either before or a minimum of 12
months after the ablation procedure. The MRI
was obtained with a Magnetom Vision (Siemens,
Germany) system. Using a breath-hold technique
the static images were obtained as T1-weighted
spin echo and T2-weighted STIR scans. Cine images
were obtained using cardiac-gated sequences.
Clinical and electrophysiological differences between patients
The MRI was reported by a single cardiac radiolo-
gist blinded to the clinical details. Each study was
examined for abnormalities in the morphology of
the right and left ventricle. Measurements of right
ventricular free wall thickness were made with
focal thinning defined as a wall thickness of less
than 2 mm. Fatty deposition was defined as high
intensity intramyocardial lesions on T1-weighted
images, the presence and extent of fatty deposition
was recorded. Cine studies evaluated wall motion
with areas of hypokinesis, dyskinesis or aneurysm
formation noted.
MRI abnormalities considered major included
right ventricular dilatation, wall motion abnor-
malities, diffuse right ventricular wall thinning
and diffuse fatty infiltration. Focal areas of right
ventricular wall thinning or fatty infiltration
of less than 2 cm2 were defined as minor MRI
abnormalities.
Electrophysiological study
All patients gave informed consent and underwent
electrophysiological study and ablation according
to standard protocols. Anti-arrhythmic medications
and warfarin were discontinued 5 days prior to the
procedure. Two quadrapolar catheters were placed
into the right ventricle, at the apex and in the
outflow tract.
Programmed electrical stimulation was per-
formed from the right ventricular apex using an
eight beat drive of 600 ms with up to five extra-
stimuli introduced sequentially until refractory
levels were reached or ventricular tachycardia was
induced. Inducible monomorphic tachycardia was
considered significant and recorded.
Following programmed electrical stimulation,
isoprenaline was commenced and the dose titrated
until the sinus rate had increased by 50% or was
greater than 120 beats min−1; this was repeated
twice with a washout phase of 5 min. Spontaneous
tachycardia and repetitive monomorphic ventricu-
lar beats were recorded (Fig. 1). Programmed
electrical stimulation was repeated during the
second isoprenaline infusion. In the absence of
tachycardia, ventricular pacing consisting of 20
beat bursts, reducing from 400 ms to 240 ms in
20 ms intervals was performed and the reliance of
induction on specific cycle lengths noted.
A minimum of 30 sites in the right ventricle
were mapped in sinus rhythm to detect areas of
inhomogeneous activation and slow conduction.
Fragmented electrograms were defined as multi-
component signals with a duration >60 ms and an
amplitude of <1.5 mV.17
803
Ablation procedure
During sustained tachycardia, activation and en-
trainment mapping18 were performed to localize
the tachycardia circuit. If sustained tachycardia
could not be induced, the area of interest was
mapped in sinus rhythm observing for fragmented
electrograms and utilizing pacemapping.19 The
ablation strategy involved point ablation for
patients with triggered automatic behaviour.
Linear ablation, targeting the diastolic pathway
and exit, was attempted in patients demonstrating
features of re-entry.20 Ablation was performed
using standard 4 mm tip catheters, temperature
limited to 60 degrees. Ablation was performed for
60–120 s at each site.
Procedural success
Procedural success was defined as the absence of
any inducible tachycardia at the end of the ablation
procedure using both programmed stimulation
and isoprenaline. A partial success was defined as
successful ablation of the clinical tachycardia but
inducible non-clinical tachycardias.
Follow-up
All patients were followed-up at pre-specified in-
tervals of 1, 6 and 12 months and then yearly. In
addition, final follow-up data was collected in
October 2001. At each review, patients completed
standardized questionnaires regarding symptoms
and underwent a standard 12-lead electrocardio-
gram, 48-h ambulatory electrocardiographic re-
cordings and transthoracic echocardiography.
Results of implantable cardioverter defibrillator
interrogations, unscheduled outpatients appoint-
ments and hospital admissions were also collected.
Statistical analysis
Continuous variables are expressed as mean±
standard deviation. Continuous variables were
compared using a two tailed t-test. Discrete vari-
ables were compared using a Chi-squared test,
unless the variable being analysed had fewer than
five occurrences, in which case a Fisher's exact test
was used. P<0.05 was considered significant.
Results
Demographic data
The study comprised 50 patients, 22 males, with a
mean age of 40 (range 17–56). Seventeen of the
804 D. O'Donnell et al.
Clinical and electrophysiological differences between patients 805

Table 1 Clinical characteristics of enrolled patients Table 2 Structural abnormalities

ARVD RVOT P value ARVD RVOT P value
Number 17 33 TTE—RV dilatation 6 (35%) 0 <0.01
Age 40±10 39±9 ns TTE—RV RWMA 2 (12%) 0 ns
Male 11 (65%) 11 (33%) ns MRI—RV dilatation 8 (47%) 0 <0.01
Syncope 8 (47%) 13 (39%) ns MRI—RV RWMA 11 (65%) 1 (3%) <0.01
Exercise potentiation 10 (59%) 26 (79%) ns MRI—Fat >2 cm2 9 (53%) 1 (3%) <0.01
Family history 9 (53%) 0 <0.01 MRI—Fat <2 cm2 7 (41%) 13 (42%) ns
ECG depolarization 5 (30%) 0 <0.01 MRI—Thinning >2 cm2 10 (59%) 1 (3%) <0.01
ECG repolarization 6 (36%) 2 (6%) =0.03 MRI—Thinning <2 cm2 7 (41%) 11 (33%) ns
Arrhythmias 17 (100%) 33 (100%) ns Major MRI findings 15 (88%) 2 (6%) <0.01
Structural Minor MRI findings 2 (12%) 16 (48%) =0.02
Major 7 (41%) 0 >0.01 No abnormalities 0 15 (45%) <0.01
Minor 7 (41%) 1 (3%) <0.01
ARVD=arrhythmogenic right ventricular dysplasia; RVOT=
Number of major criteria 1.2 0.0 <0.01
right ventricular outflow tract tachycardia; TTE=
Number of minor criteria 3.0 1.1 <0.01
transthoracic echocardiogram; RV=right ventricle; RWMA=
Family history, ECG depolarization and repolarization regional wall motion abnormality; MRI=magnetic resonance
abnormalities, arrhythmias, structural and major and imaging. Major MRI findings=right ventricular wall motion
minor criteria are all defined according to the Study abnormality, right ventricular dilatation, fatty infiltration
Group on Arrhythmogenic Right Ventricular Dysplasia/ >2 cm2 or focal thinning >2 cm2. Minor MRI findings=fatty
Cardiomyopathy of the Working Groups on Myocardial and infiltration <2 cm2 or focal thinning <2 cm2.
Pericardial Disease and Arrhythmias of the European
Society of Cardiology and of the Scientific Council on
Cardiomyopathies of the World Heart Federation.12
ARVD=arrhythmogenic right ventricular dysplasia; RVOT=
right ventricular outflow tract tachycardia; ns=not
significant. sion in the right precordial leads (V1–V3) was seen in
36% of patients with ARVD and 6% of patients with
RVOT tachycardia. Late potentials on the signal
averaged electrocardiogram were not present in
patients were classified as ARVD and 33 as RVOT any patient with RVOT tachycardia but were
tachycardia. The demographic, structural, electro- present in 78% of the patients with ARVD (Figs. 2
cardiographic and clinical data is detailed in Tables and 3).
1 and 2. All patients had ventricular tachycardia or re-
There were no significant differences in symp- peated monomorphic ventricular ectopic beats
toms between patients with ARVD and RVOT tachy- documented on electrocardiogram. In all cases a
cardia. The mode of presentation was syncope or left bundle branch block pattern was present. All
collapse in 42% and palpitations in the remaining patients with RVOT tachycardia and nine (53%) of
58%. Exercise potentiation of symptoms was re- the patients with ARVD demonstrated an inferior
ported in 26 (79%) of the RVOT tachycardia patients axis during tachycardia. The remaining patients
and in 10 (59%) patients with ARVD. Almost 60% of with ARVD demonstrated a normal or superior axis
patients with ARVD had a family member with ARVD during tachycardia. Seven patients (42%) with ARVD
or a family history of premature sudden cardiac but none with RVOT had more than one morphology
death. None of the RVOT tachycardia patients had a of documented clinical tachycardia.
family history of tachycardia.
Structural assessments
Electrocardiographic analysis
Transthoracic echocardiograms detected structural
The routine electrocardiogram was abnormal in 52% abnormalities in seven (42%) patients with ARVD.
of patients with ARVD and in 6% of patients with Major MRI abnormalities were present in 15 (88%)
RVOT tachycardia. Thirty percent of the patients ARVD patients. All patients with echocardiographic
with ARVD displayed epsilon waves, incomplete abnormalities also had major abnormalities on MRI
right bundle branch block or a localized prolonga- scans. The remaining two (12%) ARVD patients dem-
tion of the QRS complex in V1 or V2. T wave inver- onstrated minor abnormalities only on MRI scans.

Fig. 1 (a,b) An example of two different morphologies of ventricular tachycardia that were both seen clinically in a patient with
ARVD. (c) An example of monomorphic ventricular ectopic beats which were induced with isoprenaline in a patient with RVOT
tachycardia.
806
Fig. 2 (a) Example of normal electrograms in the right ventricular outflow tract of a patient with ARVD. The recordings are at a paper
speed of 100 mm s−1. The mapping electrodes are recorded with a gain of 1000. (b) Example of fragmented electrograms in the right
ventricular free wall of the same patient with ARVD. The recordings are at a paper speed of 100 mm s−1. The mapping electrodes are
recorded with a gain of 2500.
Fig. 3 Kaplan–Meier curve of freedom from ventricular tachy-
cardia. Cumulative rates of freedom from ventricular tachy-
cardia (VT) recurrence comparing patients with arrhythmogenic
right ventricular dysplasia (-%-) and right ventricular outflow
——
tract tachycardia ( ).
Structural abnormalities were detected on MRI
scans in 18 (54%) patients with RVOT tachycardia
but no echocardiographic abnormalities were
present. The MRI abnormalities were considered
major in two (6%) and minor in the remaining 16
(48%).
D. O'Donnell et al.
Right ventricular cine angiography was per-
formed at the discretion of the cardiologist in 23
patients, 11 with ARVD and 12 with RVOT. This was
reported as abnormal in seven patients with ARVD,
but none with RVOT.
Electrophysiological study and
radiofrequency ablation
Ventricular tachycardia was inducible with pro-
grammed electrical stimulation in 14 (82%) patients
with ARVD, but in only one (3%) with RVOT tachy-
cardia. All with RVOT tachycardia had ventricular
tachycardia or frequent monomorphic ventricular
ectopic beats during isoprenaline infusion. Ven-
tricular tachycardia was sustained, defined as
lasting longer than 30 s, in 12 (71%) of the ARVD
patients and in five (15%) of the RVOT tachycardia
group.
The ARVD patients had an average of 1.8 mor-
phologies of inducible ventricular tachycardia
(range 1–6), with 12 (71%) demonstrating more
than one morphology (Table 3). At least one of
the induced morphologies matched the clinical
ventricular tachycardia in all patients. All RVOT
Clinical and electrophysiological differences between patients 807

Table 3 Electrophysiological studies

ARVD RVOT P value
Inducible with PES 14 (82%) 1 (3%) <0.01
Inducible with isoprenaline 3 (18%) 27 (81%) <0.01
Monomorphic VEBs only 1 (6%) 6 (18%) ns
Sustained tachycardia 12 (71%) 5 (15%) <0.01
Number of VT morphologies l.8±0.8 1.0±0.1 <0.01
Greater than one VT morphology 12 (71%) 0 <0.01
Fragmented potentials 14 (82%) 1 (3%) <0.01
Number of ablations 15±5 8±3 =0.05
Successful procedure 8 (48%) 32 (97%) <0.01
Follow-up (months) 58±18 54±17 ns
Recurrent VT 8 (48%) 2 (6%) <0.01
ARVD=arrhythmogenic right ventricular dysplasia; RVOT=right ventricular outflow tract tachycardia; VT=ventricular tachycardia;
PES=programmed electrical stimulation; VEB=ventricular ectopic beat. Sustained tachycardia >30 s; ns=not significant.

tachycardia patients demonstrated only a single Follow-up

morphology of ventricular tachycardia or ventricu-
lar ectopic beats, which was identical to that re-
corded clinically. The mean cycle length of
ventricular tachycardia was 360 ms (265–440 ms) in
the RVOT patients and 310 ms (230–420 ms) in the
ARVD patients.
Mapping of the right ventricle revealed frag-
mented potentials in the majority of patients
with ARVD and only in a single patient with RVOT
tachycardia. The sites of the fragmented potentials
correlated poorly with successful ablation sites.
The successful ablation sites in the RVOT
patients had a mean pre-systolic activation of 28 ms
(13–48 ms) and this was greater than 30 ms in 18
patients. In the ARVD group, concealed entrain-
ment was demonstrated for 15 different ventricular
tachycardias in 12 patients. Fragmented electro-
grams and diastolic potentials guided ablation
in the remaining patients. The mean number of
ablations per procedure was 10; the number of
ablations in the ARVD patients (mean 18, range
7–38) was significantly greater than in the
RVOT tachycardia patients (mean 6, range 1–22)
(P<0.01).
The mean follow-up was 56 months (13–92
months), and all patients were followed-up for a
minimum of 12 months. Recurrence of ventricular
tachycardia was documented in eight (47%) of the
ARVD patients and two (6%) of the RVOT tachy-
cardia patients. Recurrence in the RVOT tachy-
cardia patients followed a successful procedure in
one patient and an unsuccessful procedure in the
other. In the ARVD patients, recurrence followed a
complete or partially successful procedure in three
patients and in five patients with an unsuccessful.
No patients died during the follow-up period.
Two of the ARVD patients had an implantable
cardioverter defibrillator prior to the procedure
and an additional six patients received a defibrilla-
tor following the procedure. Fifteen of the ARVD
patients, including all patients who were not
treated with an implantable cardioverter defibril-
lator, were maintained long-term on sotalol (4) or
amiodarone (11). None of the patients with RVOT
received an implantable cardioverter defibrillator
or class 3 anti-arrhythmic agents. The RVOT patient
who failed ablation was discharged on atenolol.

Acute success Outcome in patients with MRI abnormalities

Acute procedural success was achieved in 32 (97%)
and failure in one (3%) of the RVOT patients. Acute
success was achieved in seven (41%) of the ARVD
patients with a partial success in five (29%) and
failure in five (29%).
There were no significant differences in demo-
graphic, electrophysiological or conduct of ablation
between patients with a procedural success or
failure.
The presence of MRI abnormalities in the patients
with RVOT tachycardia did not have a significant
effect on acute procedural success. The procedure
was successful in 17/18 with MRI abnormalities and
15/15 without MRI abnormalities (P⫽ns).
Recurrent ventricular tachycardia was seen in
two RVOT tachycardia patients; one patient with
MRI abnormalities and an unsuccessful initial
procedure, and one with asymptomatic recurrence
808
Table 4 Relationship of MRI findings in patients with right ventricular outflow tract tachycardia to acute and long-term success
of radiofrequency ablation
Number
Overall 33
MRI abnormality 18 (54%)
No MRI abnormality 15 (46%)
following an initially successful procedure in a
patient without MRI abnormalities (Table 4). The
patient with the initial failed procedure had a
successful repeat procedure using an irrigated
tip catheter. The patient with an asymptomatic
recurrence declined a further procedure.
Discussion
This study compared 50 consecutive patients with
ARVD or RVOT tachycardia, using traditional diag-
nostic tools, MRI and invasive electrophysiological
features and correlated these with procedural
success and long-term outcome following radio-
frequency ablation. The major findings of the study
are firstly that ARVD and RVOT tachycardia are
different electrophysiological syndromes. Regard-
less of results from non-invasive investigations,
electrophysiological findings can independently
differentiate the two diagnoses on the basis of the
mechanism of induction, the number of ventricular
tachycardia morphologies and fragmented electro-
grams. And secondly, that in RVOT tachycardia the
presence of minor abnormalities on MRI has no
impact on electrophysiological properties, ablation
success or long-term recurrence of ventricular
tachycardia.
Invasive electrophysiology study
This report has demonstrated that invasive electro-
physiological findings can differentiate ARVD and
RVOT tachycardia. In this study ventricular tachy-
cardia was inducible by programmed electrical
stimulation in 82% of the patients with ARVD, but in
only 3% of those with RVOT tachycardia. Conversely
tachycardia was uniformly inducible with isoprena-
line and cycle length dependent in the patients
with RVOT tachycardia. Seventy percent of the
patients with ARVD had more than one morphology
of inducible ventricular tachycardia and the major-
ity had significant zones of fragmented electro-
grams, whereas all RVOT tachycardia patients had
only a single morphology of ventricular tachycardia
and fragmented electrograms were rarely seen.
D. O'Donnell et al.
Acute success Recurrent VT
32 (97%) 2 (6%)
17 (95%) 1 (5%)
15 (100%) 1 (5%)
These electrophysiological findings suggest sig-
nificant differences in underlying disease process
between ARVD and RVOT patients. Arrhythmia in-
duction with programmed electrical stimulation
particularly in the presence of fragmented electro-
grams favours re-entry as the predominant mech-
anism for tachycardia in ARVD patients. Induction
of ventricular tachycardia by isoprenaline with cy-
cle length dependence is consistent with a
cyclic—AMP mediated triggered activity being the
predominant mechanism in RVOT tachycardia.21
The more extensive disease process evidenced
by zones of fragmented electrograms contributes to
the different ventricular tachycardia morphologies
seen in individual ARVD patients.
The findings at electrophysiological study clearly
differentiate the two diagnoses on the basis of
their different arrhythmic mechanisms. This allows
accurate identification of patients who will be
cured by ablation and remain free from recurrence
or progression of tachycardia.
Structural information
With advances in technology, non-invasive imaging
has become more sensitive in detecting right ven-
tricular structural abnormalities. In this study, MRI
detected twice as many structural abnormalities in
the ARVD patients than a combination of trans-
thoracic echocardiography and right ventricular
cine angiography. None of the RVOT tachycardia
patients had structural abnormalities on echocardi-
ography or angiography. However, MRI detected
abnormalities in 54%. Similar rates of MRI abnor-
malities in patients with RVOT tachycardia have
previously been reported.12–15
The extent of MRI abnormality also differed be-
tween patients with ARVD and RVOT tachycardia.
Major structural abnormalities were seen on MRI in
88% of patients with ARVD but in only 6% of those
with RVOT tachycardia. Minor abnormalities only
were detected in the remaining 12% of ARVD
patients and in 48% of patients with RVOT
tachycardia.
Clinical and electrophysiological differences between patients
In this report the electrophysiological character-
istics did not correlate with the presence or ab-
sence of abnormalities on MRI. Mode of tachycardia
induction, presence of fragmented signals and
number of ablations in the RVOT tachycardia
patients was similar whether MRI abnormalities
were present or not. The presence of abnormalities
on MRI did not have any bearing on acute or the
longer term success or subsequent recurrence of
ventricular tachycardia following ablation.
The finding of a degree of structural abnormality
on MRI has led to speculation that RVOT tachycardia
may be an early form of ARVD with the same
potential for disease progression. However, studies
to date have failed to show evidence of disease
progression during follow-up of patients with
RVOT tachycardia.16,22 This analysis supports the
previous findings, with no evidence of disease pro-
gression or arrhythmia recurrence during follow-up
following ablation.
Previous studies
This analysis supports the conclusions of others that
ARVD and RVOT tachycardia are fundamentally
different entities that can usually be distinguished
clinically.1,2,6,23 Major abnormalities on standard
electrocardiograms, signal-averaged electrocardio-
grams or transthoracic echocardiography are
hallmarks of ARVD.
Contrary to previous reports, frequency of symp-
toms and history of syncope were similar in ARVD
and RVOT tachycardia.1,24 This study enrolled only
patients referred for electrophysiological evalua-
tion and this has introduced selection bias into
the sample. The patients enrolled in the study
probably represent the more symptomatic end of
the RVOT tachycardia spectrum. This may have
blunted any expected differences in symptom
frequency between the two groups.
The procedural success rates and ventricular
tachycardia recurrence rates in this report are in
keeping with previously published figures. Ablation
is rarely curative of all arrhythmias in ARVD; the
acute success rate is reported to be less than 40%
with high later recurrence rates over time due
to the progressive nature of the disease.25,26 The
success rate of ablation in the ARVD patients in this
study was 42% and the recurrence rate 48% over 58
months of follow-up. Ablation for RVOT tachy-
cardia, on the other hand, is traditionally thought
to be curative in the majority of patients and the
acute success rate of 97% and long-term success
rate of 94% in this report is expected.20,22
809
Clinical implications
The importance of electrophysiological findings in
predicting arrhythmia mechanism and long-term
outcome should assist in recommending ongoing
therapy following radiofrequency ablation. Even in
the presence of minor structural abnormalities
ablation is curative in the majority of patients
with features of RVOT and a focal arrhythmia mech-
anism.
Recurrent ventricular tachycardia is seen in
almost half of the patients with ARVD following an
ablation procedure; 19% after a successful proce-
dure and 100% following an unsuccessful procedure.
The recurrence of ventricular tachycardia after a
successful procedure in ARVD is significantly higher
than after successful ablation of RVOT or even
ventricular tachycardia associated with ischaemic
heart disease.27 The inability of a successful proce-
dure to reliably protect against ventricular tachy-
cardia recurrence in ARVD patients suggests that
ablation should be reserved for patients with highly
symptomatic episodes and considered an adjunct to
implantable cardioverter defibrillators.
This study in part attempted to address the issue
of disease progression amongst RVOT tachycardia
patients. Whilst no evidence of disease progression
was documented, the rate of progression in ARVD is
unknown and may be highly variable.28 The
follow-up in this study may be insufficient and
serial evaluations over a longer time frame would
be needed to definitively answer the question of
progression.
Conclusions
This analysis shows that ARVD and RVOT tachy-
cardia can be differentiated clearly on the basis
of electrophysiological characteristics. The findings
suggest the two conditions behave as fundamen-
tally different entities.
The presence of minor structural abnormalities
on MRI in RVOT tachycardia patients is consistent
with benign natural history, high ablation success
rates and low later ventricular tachycardia
recurrence.
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